Abstract. The pathogenesis of Sendai virus infection was studied in genetically immunodeficient mice of genotype scidlscid. bglbg (SCID-beige) using C.B-17 SCID-beige mice, a BALB/c-related strain that expresses the same major histocompatibility complex as the Sendai virus-susceptible DBA/2 (H-2d). Mice were inoculated intranasally with isolate 771076 of Sendai virus, then killed at 2-day intervals beginning on day 4 postinoculation. Clinical signs were evident beginning at 8 to 10 days post-inoculation, and all animals remaining were killed in extremis by 14 to 17 days post-inoculation. Lesions in inoculated mice were confined to the respiratory tract. In the nasal passages, a nonresolving rhinitis, with epithelial hyperplasialmetaplasia occurred. Cranioventral bronchopneumonitis was characterized by marked hyperplasia and necrosis of epithelial cells lining airways and with leukocytic infiltration. At the alveolar level, there was marked hypertrophy and hyperplasia of type I1 pneumocytes, mobilization of alveolar macrophages, and obliteration of the normal architecture in severely affected areas. Viral antigen was evident beginning at 4 days post-inoculation and persisted in affected areas throughout the duration of the study. Because immunocompetent C57BLl6 mice are known to be genetically resistant to Sendai virus, the susceptibility of C57BL/6 SCID-beige to Sendai virus was then compared to that of C.B-17 SCID-beige mice. In age-matched animals of the two strains, there was no evidence of natural resistance to Sendai virus infection in the immunodeficient C57BL/6 strain compared to the C.B-17 mice. These studies indicate that the genetic differences in susceptibility of two strains of immunocompetent mice to Sendai virus infection are eliminated by expression of the mutations scid and beige.

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